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FBF represses the Cip/Kip cell-cycle inhibitor CKI-2 to promote self-renewal of germline stem cells in C. elegans
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
 
ID 4488942
Author(s) Kalchhauser, Irene; Farley, Brian M.; Pauli, Sandra; Ryder, Sean P.; Ciosk, Rafal
Author(s) at UniBasel Adrian-Kalchhauser, Irene
Year 2011
Title FBF represses the Cip/Kip cell-cycle inhibitor CKI-2 to promote self-renewal of germline stem cells in C. elegans
Journal The EMBO Journal
Volume 30
Number 18
Pages / Article-Number 3823-9
Keywords Animals;Caenorhabditis elegans Proteins/antagonists & inhibitors/metabolism;Caenorhabditis elegans/physiology;Cell Cycle;Cells, Cultured;Cyclin-Dependent Kinase Inhibitor Proteins/antagonists & inhibitors;Gene Expression Regulation;RNA-Binding Proteins/metabolism;Stem Cells/physiology
Mesh terms Animals; Caenorhabditis elegans, physiology; Caenorhabditis elegans Proteins, metabolism; Cell Cycle; Cells, Cultured; Cyclin-Dependent Kinase Inhibitor Proteins, antagonists & inhibitors; Gene Expression Regulation; RNA-Binding Proteins, metabolism; Stem Cells, physiology
Abstract Although the decision between stem cell self‐renewal and differentiation has been linked to cell‐cycle modifications, our understanding of cell‐cycle regulation in stem cells is very limited. Here, we report that FBF/Pumilio, a conserved RNA‐binding protein, promotes self‐renewal of germline stem cells by repressing CKI‐2Cip/Kip, a Cyclin E/Cdk2 inhibitor. We have previously shown that repression of CYE‐1 (Cyclin E) by another RNA‐binding protein, GLD‐1/Quaking, promotes germ cell differentiation. Together, these findings suggest that a post‐transcriptional regulatory circuit involving FBF and GLD‐1 controls the self‐renewal versus differentiation decision in the germline by promoting high CYE‐1/CDK‐2 activity in stem cells, and inhibiting CYE‐1/CDK‐2 activity in differentiating cells.
Publisher EMBO Press
ISSN/ISBN 0261-4189 ; 1460-2075
edoc-URL https://edoc.unibas.ch/69890/
Full Text on edoc No
Digital Object Identifier DOI 10.1038/emboj.2011.263
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/21822213
Document type (ISI) Journal Article
 
   

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